ArticleFrontiers in pharmacology2025
Cisplatin induces hippocampal neurotoxicity and cognitive impairment in rats through neuroinflammation, oxidative stress, and overexpression of glutamatergic receptors mRNA.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Barbaloin Attenuates Cisplatin-Induced Hippocampal Neurotoxicity by Suppressing Oxidative Stress, Neuroinflammation, and Apoptosis: In Vivo and In Silico Evidence.Journal of biochemical and molecular toxicology · 2026Article
- Morphological and Biochemical Changes in Rat Hippocampal Tissue Following Exposure to Different Doses of Cisplatin.Brain sciences · 2026Article
- Glycine as a potential neuroprotective adjuvant to reduce cisplatin-induced brain inflammation in mice.BMC neuroscience · 2026Article
- The role of oxidative stress and antioxidant therapy in cisplatin neurotoxicity: preclinical evidence in the last decade.Archives of toxicology · 2026Review
- Neuroprotective effects of glycine against cisplatin-induced cognitive decline in mice.Annals of medicine and surgery (2012) · 2026Article
- The hepatoprotective role of piperazine ferulate against cisplatin-induced hepatotoxicity in rats: insights into the Keap1/Nrf-2/HO-1 signaling and inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sacubitril/Valsartan Fails to Ameliorate Cisplatin-Induced Cognitive Impairment.Drug design, development and therapy · 2026Article
- Loss of KLF15 expression characterizes proximal tubule injury in cisplatin-induced acute kidney injury: A multi-omics study.Current research in toxicology · 2026Article
- The lack of efficacy of tirzepatide in mitigating cisplatin-induced neurotoxicity and cognitive impairment in rats.Frontiers in toxicology · 2026Article
- Sacubitril/valsartan mitigates cisplatin-induced liver injury through modulation of oxidative stress, Caspase-3 activity, and RXR-α signaling in experimental rats.Frontiers in pharmacology · 2026Article
- Protective potential of tween 80-functionalized chitosan-selenium nanoparticles containing quercetin against cisplatin neurotoxicity in PC12 cells: an in vitro and network pharmacology study.Scientific reports · 2025Article
- Altered effective connectivity within the hippocampal-prefrontal circuit in patients with non-small cell lung cancer after platinum chemotherapy.Brain imaging and behavior · 2025Article
- Protective effects of avenanthramide-C against cisplatin-induced cardiotoxicity in rats by attenuating oxidative stress, inflammatory cytokines, and modulating p62-Keap1-Nrf2 pathway.Frontiers in pharmacology · 2025Article
- Ameliorative Effect of Empagliflozin and Linagliptin on Cisplatin-Induced Nephrotoxicity and Cardiotoxicity by Reducing Oxidative Stress.Drug design, development and therapy · 2025Article
- Integrative Metabolomics and Ionomics Identify Organ-Specific Responses Associated with Cisplatin Treatment in Mice.Drug design, development and therapy · 2025Article
- Avenanthramide C mitigates cisplatin-induced hippocampal neurotoxicity and cognitive impairment in rats via suppression of neuroinflammation and neuronal apoptosis.Frontiers in pharmacology · 2025Article
- Exploring how levetiracetam mitigates toxicity and ameliorates memory impairment.Frontiers in pharmacology · 2025Review
- [Chemotherapy-related central nervous system injury in children with acute lymphoblastic leukemia: research progress].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatricsReview
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Authors and funding
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Abstract
Chemotherapy-induced cognitive deficits are a prevalent adverse effect in patients with cancer undergoing chemotherapy. We investigated cisplatin-induced neurotoxicity by assessing neuroinflammation and expression of glutamate receptors. Two groups of eight-week-old rats (n = 10 per group) were used: control and cisplatin-treated. Cisplatin (8 mg/kg, i. p.) was administered each 2 days for three cycles. From rats hippocampi, we measured: concentrations of nuclear factor-kappa B (NF-κB), tumor necrosis factor (TNF)-α, and interleukin (IL)-6); mRNA countenance of synapse-related proteins (α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) and N-methyl-D-aspartic acid receptors (NMDARs); levels of reactive oxygen species (ROS), nuclear factor erythroid 2-related factor 2 (Nrf-2), superoxide dismutase (SOD); mitochondrial complex I (MCI) activity; lipid peroxidation. The cisplatin group exhibited significant reductions in survival rate to 40% and body weight, confirming the initiation of cisplatin toxicity. In contrast with the control group, the cisplatin group exhibited notably increased hippocampal levels of pro-inflammatory substances (NF-κB, TNF-α, IL-6), synapse-related proteins (AMPARs, NMDARs), and oxidative-stress mediators (ROS, Nrf-2, SOD). Cisplatin treatment resulted in declined MCI activity and increased lipid peroxidation. These findings indicate that cisplatin-induced cognitive impairment may be mediated by heightened hippocampal neuroinflammation and overactivation of glutamatergic receptors.
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